Prolonged midazolam elimination half‐life.

Dundee, J. W.; Collier, P. S.; Carlisle, R. J. T.; Harper, K. W.

doi:10.1111/j.1365-2125.1986.tb05217.x

Cited by 86 publications

(29 citation statements)

References 14 publications

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“…Dundee et al (1986) and Dundee (1987) inferred that there exists a subpopulation of poor metabolizers of midazolam because midazolam is primarily metabolized by oxidation to a-OH-midazolam and their finding of a 6.5% (14 of 217) incidence of prolonged tl½ in an otherwise healthy population coincides with the well known incidences of poor metabolizers reported for other drugs. In contrast, Kassai et al (1988) and Klotz et al (1986) have presented convincing evidence that the formation of a-OH-midazolam is not subject to known genetic polymorphisms.…”

Section: Introductionmentioning

confidence: 72%

“…Several recent reports have discussed the explanation for the prolonged tl½ (> 7 h) of midazolam in a small number of subjects or patients (Dundee et al, 1986;Dundee, 1987;Kassai et al, 1988;Klotz et al, 1986;Klotz, 1987). Dundee et al (1986) and Dundee (1987) inferred that there exists a subpopulation of poor metabolizers of midazolam because midazolam is primarily metabolized by oxidation to a-OH-midazolam and their finding of a 6.5% (14 of 217) incidence of prolonged tl½ in an otherwise healthy population coincides with the well known incidences of poor metabolizers reported for other drugs.…”

Section: Introductionmentioning

confidence: 99%

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Increased volume of distribution prolongs midazolam half‐life.

Wills

Khoo

Soni

et al. 1990

Brit J Clinical Pharma

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It has recently been shown by several investigators that the half-life (t½,) of midazolam is prolonged (> 7 h) in a small proportion of the population. One group has inferred that this subpopulation represents a group of slow metabolizers of midazolam to ot-OH-midazolam. Others disagree and postulate that there is an increase in the volume of distribution (V) resulting in a prolonged t/2. This controversy led us to report experience from 90 subjects and patients where t½/2, V, and clearance (CL) were determined by both model-dependent and -independent pharmacokinetic analysis. We found a 5.6% (5 of 90) incidence of prolonged t½/2, similar to that previously reported. V was clearly increased without a decrease in CL in the five subjects with prolonged t½/2. Thus, the prolonged t/2 is secondary to an increase in V and not a result of alterations in CL and metabolism.

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Section: Introductionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Increased volume of distribution prolongs midazolam half‐life.

Wills

Khoo

Soni

et al. 1990

Brit J Clinical Pharma

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“…The plasma concentrations of midazolam, ahydroxymidazolam and a-hydroxymidazolam glucuronide in patients 2, 3, 4, 5 and 6 during the anhepatic period and following reperfusion are shown in Figure 1 (Mahon et al, 1977)), the kidney (which has been implicated in the metabolism of morphine (Moore etal., 1986)), and the lung (Heizman et al, 1983 (Brown et al, 1979;Dundee et al, 1980Dundee et al, , 1986Greenblatt et al, 1981 and. The duration of the anhepatic period is necessarily short and the calculated half-life may therefore represent a distribution rather than an elimination half-life. Caution in the application of these results to patients with severe liver failure is necessary.…”

Section: Resultsmentioning

confidence: 99%

Extra‐hepatic metabolism of midazolam.

Manara

Dawling

1989

Brit J Clinical Pharma

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Six patients received 10 mg of midazolam intravenously during the anhepatic period of liver transplantation. Arterial blood was sampled during this time and for a similar period following revascularisation. The plasma was analysed using gas chromatography and electron capture detection (GC-ECD) for midazolam a-hydroxymidazolam and ahydroxymidazolam glucuronide. Five of the six patients had small but significant concentrations of metabolites detected during the anhepatic period, demonstrating the presence of extra-hepatic sites of metabolism for this drug. The remaining patient had plasma concentrations of metabolites below the lower limit of detection (2,ug 1-1). This may represent a pharmacogenetic abnormality or a temporary failure of midazolam metabolism secondary to the patients illness affecting the extra-hepatic sites of metabolism.

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“…Benzodiazepines are metabolised in the liver via the cytochrome P450 (CYP) 3A4 and 3A5 system and excreted mainly in the urine. Due to natural variability in this system among various populations, the elimination half-life of these drugs may be prolonged in 5-8% of the population [38]. Midazolam has a large volume of distribution similar to diazepam but a short elimination half-life (2 h) and faster onset of action [18].…”

Section: Benzodiazepinesmentioning

confidence: 99%

Sedation for flexible bronchoscopy: current and emerging evidence

José¹,

Shaefi²,

Navani³

2013

European Respiratory Review

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Flexible bronchoscopy is commonly performed by respiratory physicians and is the gold standard for directly visualising the airways, allowing for numerous diagnostic and therapeutic interventions. With the widespread use of flexible bronchoscopy and the evolution of interventional bronchoscopy with more complex and longer procedures, physicians are placing increasing importance on the use of sedation as a necessary adjunct to topical anaesthesia. There is no standardised practice for the use of sedation in bronchoscopy with a good deal of variation among physicians regarding the use of pre-procedure medication and pharmacological sedatives. In addition, there is ongoing debate and controversy about proceduralist-administered versus anaesthetist-administered sedation whilst at the same time there is a growing body of evidence that nonanaesthetist administered sedation is safe and cost-effective. In this review we summarise the evidence for the use of sedation as an adjunct to topical anaesthesia in bronchoscopy and provide the clinician with up-todate concise guidance for the use of pharmacological sedatives in bronchoscopy and future directions for sedation in the bronchoscopy suite.

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Prolonged midazolam elimination half‐life.

Cited by 86 publications

References 14 publications

Increased volume of distribution prolongs midazolam half‐life.

Increased volume of distribution prolongs midazolam half‐life.

Extra‐hepatic metabolism of midazolam.

Sedation for flexible bronchoscopy: current and emerging evidence

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